During the past year we attempted to define whether the pattern of stimulated insulin release by the beta cell of aging rat is the same as that of the beta cell of a young rat. Our results have shown clearly that under defined in vitro conditions which are free of systemic variables, average beta cells of aging rats secrete only a fraction of insulin secreted by average beta cells of young rats in response to two natural secretagogues. The work in progress attempts to enlarge the list of stimulating agents to determine whether the observed defect is global or unique for only those secretagogues which enter the cell and are metabolized. In addition, we will attempt to define the mechanism behind this defect; i.e., does the problem stem from a defective message or from a defective secretory process? We will attempt to understand if, and in what fashion, intact animals compensate for the deficiency of their beta cells. Finally, we will begin to define whether the observed defect relates to age itself or to age-associated problems such as obesity and lack of exercise.